During the past year, our research program has pursued studies to elucidate the molecular events associated with the development of pediatric tumors, while terminating a previously major line of investigation directed at understanding the genetic basis of transformation and tumorigenesis induced by polyoma virus. Experiments focused on studying polymoma virus induced transformation included: 1) Characterization of a post-translational modification of pp60 c-src molecules physically associated with the polyoma virus transforming protein, middle T-antigen; 2) Characterization of the interaction between the middle T-antigen encoded by the transformation defective polyoma virus mutant, NG59, and pp60 c-src; and 3) Evaluation of the effect of SV40, adenovirus and papillomavirus infection of rodent cells on pp60 c-src tyrosyl kinase activity. Experiments we have conducted to pursue our studies of pediatric tumors have included: 1) an examination of the cellular and genetic differences underlying two histiologically identical tumors: neuroblastoma and peripheral neuroepithelioma; 2) Characterization of the precise localization of the rcp(11;22) translocations found in peripheral neuroepithelioma and in a second pediatric tumor, Ewing's sarcoma; 3) Evaluation of the frequency of the rcp(11;22) translocation in pediatric solid tumors; 4) Evaluation of the importance of N-myc during the clinical progession of neuroblastoma; and 5) Evaluation of the importance of pp60 c-src activation in human cancer.